ArticleBioMed research international2020
Levosimendan Protects against Doxorubicin-Induced Cardiotoxicity by Regulating the PTEN/Akt Pathway.
Article in BioMed research international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Identifying common pathways for doxorubicin and carfilzomib-induced cardiotoxicities: transcriptomic and epigenetic profiling.Scientific reports · 2025Article
- Thiolutin Alleviates Cardiotoxic Effects of Doxorubicin by Suppressing NLRP3 Inflammasome in the Mouse Model.Cardiovascular toxicology · 2025Article
- Role of Oxidative Stress and Inflammation in Doxorubicin-Induced Cardiotoxicity: A Brief Account.International journal of molecular sciences · 2024Review
- Loss of RACK1 promotes glutamine addiction via activating AKT/mTOR/ASCT2 axis to facilitate tumor growth in gastric cancer.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- The Essential Oil fromPharmaceuticals (Basel, Switzerland) · 2022Article
- Therapeutic Targets for DOX-Induced Cardiomyopathy: Role of Apoptosis vs. Ferroptosis.International journal of molecular sciences · 2022Review
- MicroRNAs in doxorubicin-induced cardiotoxicity: The DNA damage response.Frontiers in pharmacology · 2022Review
- Levosimendan Postconditioning Attenuates Cardiomyocyte Apoptosis after Myocardial Infarction.Journal of healthcare engineering · 2022Article
- Anticancer Drug-Induced Cardiotoxicity: Insights and Pharmacogenetics.Pharmaceuticals (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsMyocyte apoptosis plays a critical role in the development of doxorubicin- (DOX-) induced cardiotoxicity. In addition to its cardiotonic effect, laboratory evidence indicates that levosimendan can inhibit apoptosis, but its role in DOX-induced cardiac injury remains unclear. Therefore, the present study is aimed at exploring whether levosimendan could attenuate DOX-induced cardiotoxicity.
methodsLevosimendan (1 mg/kg) was administered to mice through oral gavage once daily for 4 weeks, and the mice were also subjected to an intraperitoneal injection of DOX (5 mg/kg) or saline, once a week for 4 weeks, to create a chronic model of DOX-induced cardiotoxicity. A morphological examination and biochemical analysis were used to evaluate the effects of levosimendan. H9C2 cells were used to verify the protective role of levosimendan in vitro. And an Akt inhibitor was utilized to verify the cardioprotection of levosimendan.
resultsLevosimendan reduced the cardiac dysfunction and attenuated the myocardial apoptosis induced by DOX in vivo and in vitro. Levosimendan also inhibited the activation of phosphatase and tensin homolog (PTEN) and upregulated P-Akt expression both in vivo and in vitro. And inhibition of Akt abolished the cardioprotection of levosimendan in vitro.
conclusionLevosimendan may protect against DOX-induced cardiotoxicity via modulation of the PTEN/Akt signaling pathway.
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